Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

1.2K
Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is...
1.2K
Physical Properties of Amines01:26

Physical Properties of Amines

3.6K
Amines with low molecular weight are usually gaseous at room temperature, while those with high molecular weight are liquid or solids in nature. Usually, low molecular weight amines have a rotten fish-like smell. Diamines typically have a pungent smell. For instance, cadaverine and putrescine, depicted in Figure 1, are two molecules responsible for decaying tissue.
3.6K
Phase II Reactions: Acetylation Reactions01:24

Phase II Reactions: Acetylation Reactions

477
Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...
477
Titration of a Weak Acid with a Weak Base01:08

Titration of a Weak Acid with a Weak Base

3.8K
Weak acids and bases do not undergo dissociation completely, and titrations between these two are rarely studied. When such studies are performed, say, for the titration of a weak acid with a weak base, the titration curve plots the change in pH as a function of the volume of base added. Take the titration of acetic acid with ammonia, for instance. During the titration, these two species form ammonium acetate and water, but the pH change is slow and gradual.
As a result, there is no simple...
3.8K
Urea Cycle01:23

Urea Cycle

47.5K
The urea cycle describes how liver cells convert ammonia to urea. Ammonia is a toxic waste product of protein catabolism. Land animals must convert ammonia into the less toxic urea which can be safely eliminated by the kidneys through urine. Marine animals excrete ammonia directly, and the surrounding water dilutes the ammonia to safe levels.
47.5K
Prevention of Further Absorption of Poison01:14

Prevention of Further Absorption of Poison

1.0K
In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...
1.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Two fatalities from sodium azide ingestion: delayed enhanced elimination was not effective.

Clinical toxicology (Philadelphia, Pa.)·2025
Same author

Once, twice, three times a bite victim: recidivism in snake envenomation.

Clinical toxicology (Philadelphia, Pa.)·2025
Same author

Response to the letter: "Utility of electroencephalography in toxin-induced seizure".

Academic emergency medicine : official journal of the Society for Academic Emergency Medicine·2024
Same author

Utility of electroencephalography in toxin-induced seizures.

Academic emergency medicine : official journal of the Society for Academic Emergency Medicine·2024
Same author

Don't Throw the Sodium Bicarbonate Out with the Correlation.

Journal of medical toxicology : official journal of the American College of Medical Toxicology·2021
Same author

Single versus continued dosing of fomepizole during hemodialysis in ethylene glycol toxicity.

Clinical toxicology (Philadelphia, Pa.)·2020

Related Experiment Video

Updated: Nov 3, 2025

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
09:44

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

10.6K

Hyperammonemia in acetaminophen toxicity.

Ryan T Marino1,2, Alexander M Sidlak1,3

  • 1Division of Medical Toxicology, Department of Emergency Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

Clinical Toxicology (Philadelphia, Pa.)
|June 3, 2021
PubMed
Summary

In acetaminophen toxicity, high ammonia levels do not predict encephalopathy. Empiric treatment for hyperammonemia showed no benefit in patients with acetaminophen-induced liver damage.

Keywords:
Acetaminophenhepatic encephalopathyhyperammonemia

More Related Videos

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
08:47

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats

Published on: November 8, 2018

11.7K
Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model
10:40

Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model

Published on: August 4, 2012

12.8K

Related Experiment Videos

Last Updated: Nov 3, 2025

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
09:44

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

10.6K
Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
08:47

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats

Published on: November 8, 2018

11.7K
Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model
10:40

Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model

Published on: August 4, 2012

12.8K

Area of Science:

  • Hepatology
  • Toxicology
  • Neurology

Background:

  • Acetaminophen overdose can cause liver damage and elevated ammonia levels.
  • The relationship between hyperammonemia and encephalopathy in acetaminophen toxicity is not well understood.

Purpose of the Study:

  • To investigate if ammonia concentrations predict encephalopathy in acetaminophen-induced hepatotoxicity.
  • To evaluate the efficacy of empiric hyperammonemia treatment.

Main Methods:

  • Retrospective study of 102 patients with acetaminophen toxicity over 8 years.
  • Analysis of ammonia concentrations, encephalopathy grade, and treatments.
  • Calculation of sensitivity and specificity for ammonia levels predicting encephalopathy.

Main Results:

  • 75 patients had ammonia measurements; 40% exceeded 100 µmol/L.
  • Ammonia levels >100 µmol/L were neither sensitive nor specific for encephalopathy.
  • Increasing ammonia showed a small positive likelihood ratio for encephalopathy.

Conclusions:

  • Ammonia concentrations do not correlate with encephalopathy in acetaminophen-induced hepatotoxicity.
  • Alternative mechanisms may cause encephalopathy in these cases.
  • Empiric treatment for hyperammonemia did not alter patient outcomes.